Indeed, the therapeutic benefit of the dual ETAR/ETBR-antagonist is to target not only ovarian cancer cells expressing ETAR, hampering the ZEB1/miR-200 network, but also to interfere with tumor microenvironmental elements, such as cancer-associated fibroblasts, blood, lymphatic, and immune cells, tumor-associated macrophages, which mainly expressed ETBR25,28,59–61 representing a therapeutic strategy which may be used to design targeted therapies that can impair ZEB1/miR-200 transcriptional machinery in cancer cells and the complex regulatory circuits in the stromal architecture. This evidence concerns the gene EDNRA and neoplasm.